Atlas of pathophysiology, 2 Edition
Part II - Disorders
Pneumothorax is an accumulation of air in the pleural cavity that leads to partial or complete lung collapse. When the air between the visceral and parietal pleurae collects and accumulates, increasing tension in the pleural cavity can cause the lung to progressively collapse. The amount of air trapped in the intrapleural space determines the degree of lung collapse. Venous return to the heart may be impeded to cause a life-threatening condition called tension pneumothorax. Pneumothoraces are usually classified as primary spontaneous, secondary spontaneous, traumatic, or tension.
Primary spontaneous pneumothorax
· Rupture of a bleb or a bulla
Primary spontaneous pneumothorax most commonly affects tall, thin men between ages 20 and 40.
Secondary spontaneous pneumothorax
· Chronic obstructive pulmonary disease
· Cystic fibrosis
· Whooping cough
· Traumatic chest injury
· Penetrating chest trauma (stab wound, gunshot)
· Blunt chest trauma (blow from a motor vehicle accident)
· Iatrogenic chest trauma, resulting from puncture of the lung during needle aspiration lung biopsy, thoracentesis, or central venous catheter placement
· Lung collapse forced by excessive pressure
A rupture in the visceral or parietal pleura and chest wall causes air to accumulate and separate the visceral and parietal pleurae. Negative pressure is destroyed, and the elastic recoil forces are affected. The lung recoils by collapsing toward the hilus.
Open pneumothorax results when atmospheric air (positive pressure) flows directly into the pleural cavity (negative pressure). As the air pressure in the pleural cavity becomes positive, the lung collapses on the affected side, resulting in decreased total lung capacity, vital capacity, and lung compliance. Imbalances in the ventilation-perfusion ([V with dot above]/[Q with dot above]) ratio lead to hypoxia.
Closed pneumothorax occurs when air enters the pleural space from within the lung, causing increased pleural pressure, which prevents lung expansion during normal inspiration.
Tension pneumothorax results when air in the pleural space is under higher pressure than air in the adjacent lung. The air enters the pleural space from the site of pleural rupture, which acts as a one-way valve. Air is allowed to enter into the pleural space on inspiration but can't escape as the rupture site closes on expiration. More air enters on inspiration, and air pressure begins to exceed barometric pressure. Increasing air pressure pushes against the recoiled lung, causing compression atelectasis. Air also presses against the mediastinum, compressing and displacing the heart and great vessels. The air can't escape, and the accumulating pressure causes the lung to collapse. As air continues to accumulate and intrapleural pressures rise, the mediastinum shifts away from the affected side and decreases venous return. This leads to decreased cardiac output, which causes hypotension.
Signs and symptoms
· Sudden, sharp pleuritic pain exacerbated by chest movement, breathing, or coughing
· Asymmetrical chest wall movement
· Shortness of breath and respiratory distress
· Decreased vocal fremitus
· Absent breath sounds and chest rigidity on the affected side
· Subcutaneous emphysema
Tension pneumothorax produces the most severe respiratory symptoms, including:
· decreased cardiac output, hypotension, and compensatory tachycardia
· lung collapse
· mediastinal shift and tracheal deviation to the opposite side
· distended jugular veins.
Diagnostic test results
· Chest X-rays confirm the diagnosis by revealing air in the pleural space and, possibly, a mediastinal shift.
· Arterial blood gas analysis may reveal hypoxemia, possibly with respiratory acidosis and hypercapnia. Partial pressure of arterial oxygen levels may decrease at first but typically returns to normal within 24 hours.
· Bed rest
· Chest tube insertion
EFFECTS OF PNEUMOTHORAX